Biological transmission of animal and plant viruses by insect vectors is a complex and little understood process. Limited progress has been achieved in elucidating the molecular basis of persistence, cytopathology, host specificity, and the regulation of gene expression in the case of arboviruses. Even less information exists concerning these processes for the propagative plant viruses. This is unfortunate, since one propagative plant virus, wound tumor virus (WTV) is uniquely suited for studying the molecular details of virus-vector-host interactions. Like the arboviruses, WTV elicits no apparent cytopathology in its vector while infection of the host by this virus results in obvious, and often severe, disease symptoms. In addition, the WTV system offers the distinct advantage of the availability of mutant populations of virus that are impaired in the ability to replicate in, and thus be transmitted by the vector. These mutants retain the ability to replicate and produce disease symptoms in the plant host. Associated with the loss of transmissibility of WTV are delection mutation events in 4 of 12 WTV double stranded RNA genome segments. Preliminary evidence suggests the possibility that two of these four genome segments code for nonstructural viral polypeptides which may be required for WTV multiplication in the vector cell but are nonessential for WTV multiplication in the plant host. Using currently available methods we intend to investigate a) the regulation of viral gene expression in cultured vector cells initially and persistently infected with WTV, and b) the molecular basis for loss of transmissibility. It is anticipated that these studies will significantly further our knowledge of the molecular mechanisms involved in the complex process of transmission of viral pathogens by insect vectors.